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目的探讨多巴胺D2受体与帕金森病的运动行为学及发病间的关系。方法 C57BL/6野生型及D2受体基因敲除小鼠腹腔注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)制备帕金森病模型,爬杆实验、游泳实验观察比较两组小鼠行为学的改变,免疫荧光染色法观察小鼠中脑黑质致密部TH阳性神经元数目的变化。结果 MPTP注射后,小鼠爬杆实验时间延长,游泳实验评分降低,中脑黑质致密部TH阳性神经元数目下降(P<0.05或P<0.01);且D2受体基因敲除小鼠的行为学改变及TH神经元数目的减少较野生型小鼠更为明显(P<0.05或P<0.01)。结论多巴胺D2受体在小鼠肢体运动协调方面起着重要作用,D2受体缺失加剧了MPTP诱导的小鼠帕金森病样改变。
Objective To investigate the relationship between dopamine D2 receptor and motor behaviors and the pathogenesis of Parkinson’s disease. Methods Parkinson’s disease model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL / 6 wild type and D2 receptor knockout mice. The changes of behavior in the two groups of mice were observed by swimming experiment. The number of TH-positive neurons in the substantia nigra pars compacta in mice was observed by immunofluorescence staining. Results After MPTP injection, the length of climbing pole experiment in mice was prolonged, the swimming test score was decreased, the number of TH positive neurons in the substantia nigra pars compacta decreased (P <0.05 or P <0.01), and the number of D2 receptor knockout mice Behavioral changes and the decrease of TH neuron number were more obvious than those in wild type mice (P <0.05 or P <0.01). Conclusions Dopamine D2 receptor plays an important role in the coordination of limb movement in mice. Deletion of D2 receptor aggravates MPTP-induced Parkinson’s disease-like changes in mice.